Prof Mohammad Salah Abduljabbar
CEREBROVASCULAR ACCIDENT
“BRAIN ATTACK”
Objectives
 Define cerebrovascular accident and
associated terminology
 Discuss related pathophysiology and
presentation of various types of stroke
 Discuss etiology, risk factors, diagnostics,
management, and outcomes of stroke
 Review case studies and nursing diagnoses,
interventions, and goals
Definition
 Stroke or “brain attack” is an acute CNS injury
that results in neurologic Symptoms and
signs brought on by a reduction or absence of
perfusion to a territory of the brain. The
disruption in flow is from either an occlusion
(ischemic) or rupture (hemorrhagic) of the
blood vessel.
Incidence & Prevalence
 Third leading cause of death in the USA
 750,000+ people/year
 175,000 die within one year (25%)
 Leading cause of long-term disabilities
 5.5 million survivors (USA)
 15 to 30 % live with permanent disability
Stroke Statistics
 15% of adults > age 50 cannot name a single
symptom of stroke
 13 hours after onset of symptoms is the median
time to presentation
 58% of stroke patients don’t present during the
first 24 hours after onset
 52% of stroke patients in the ED are unaware
that they are experiencing a stroke
Classification
 Cerebrovascular Accident
 Ischemic Stroke
 Thrombotic
 Embolic
 Lacunar infarct
 TIA
 Hemorrhagic Stroke
 ICH
 SAH
Stroke Knowledge
 MYTHS
 FACTS
 Can’t prevent stroke
 Stroke is preventable
 Can’t treat stroke
 Stroke is treatable
 Stroke affects the heart
 Stroke is a brain attack
 Stroke affects the elderly
 Stroke affects anyone
 Recovery happens for a
 Stroke recovery occurs
few months after stroke
throughout life
Stroke: Emergency Care
Stroke Symptoms
 Sudden numbness or weakness of face, arm or leg,
especially on one side of the body
 Sudden confusion, trouble understanding or speaking
 Sudden trouble seeing in one or both eyes
 Sudden trouble walking, dizziness, loss of balance or
coordination
 Sudden severe headache with no known cause
Other Symptoms
 Sudden nausea, fever and vomiting, distinguished
from a viral illness by rapid onset (minutes or hours
vs. days)
 Brief loss of consciousness or period of decreased
consciousness
convulsions or coma)
(fainting, confusion,
Cerebral Ischemia
 Embolism
Thrombosis
 Abrupt onset
 Small vascular area
 Focal deficit
 Preceded by TIAs
 Abrupt onset
 Large vascular area
 More complex symptoms
 Acute CT normal
 Pure aphasia
 Pure hemianopia
 Acute CT normal
 High recurrence risk
Thrombotic Stroke
 Occlusion of large cerebral
vessel
 Older population
 Sleeping/resting
 Rapid event, but slow
progression (usually reach
max deficit in 3 days)
Embolic Stroke
 Embolus becomes lodged in
vessel and causes occlusion
 Bifurcations are most common
site
 Sudden onset with immediate
deficits
 Hemorrhagic
Transformation
Lacunar Strokes - 20% of all
stokes
 Minor deficits
 Paralysis and sensory loss
 Lacune
 Small, deep penetrating arteries
 High incidence:
 Chronic hypertension
 Elderly
 DIC
Lacunar Strokes
 15 – 20% of ischemic strokes
 Small penetrating branches of circle of Willis,
MCA, or vertebrobasilar artery
 Atherothrombotic or lipohyalinotic occlusion
 Infarct of deep brain structures
 Basal ganglia, cerebral white matter, thalamus,
pons, and cerebellum
 From 3 mm to 2 cm
Lacunar Stroke Syndromes
 Well-defined syndromes
 Pure motor hemiparesis (with dysarthria)
 Pure sensory stroke (loss or paresthesias)
 Dysarthria-clumsy hand (with contralateral face
and tongue weakness)
 Ataxia-hemiparesis (contralateral face and leg
weakness)
 Isolated motor-sensory stroke
 Risk factors
 Diabetes
 Hypertension
 Polycythemia
 Variable course progressing over days
 Fluctuating; progressing in steps; or remitting
 Preceded by TIAs in 25%
 Without headache or vomiting
Remember Lacunar Strokes
Transient Ischemic Attack
 “Sudden, focal neurologic deficit lasting less
than 24 hours, confined to an area of the brain
or eye perfused by a specific artery.”
 Based on assumption that TIAs do not cause
infarction or other permanent brain injury.
 Time criterion is arbitrary.
Transient Ischemic Attack
 Warning sign for stroke
 Brief localized ischemia
 Common manifestations:
 Contralateral numbness/
weakness of hand,
forearm, corner of mouth
 Aphasia
 Visual disturbancesblurring
 Deficits last less than
24 hours (usually less
than 1 or 2 hrs)
 Can occur due to:
 Inflammatory artery
disorders
 Sickle cell anemia
 Atherosclerotic changes
TIA - Differential Diagnosis
 Anxiety (panic attack)
 Migraine
 Hyperventilation
 Orthostatic hypotension
 Neuropathy (focal)
 Syncope
 Neuropathy (ischemic)
 Arrhythmias (ischemia)
 Vertigo
 Seizures
 Disequilibrium
 Conversion disorder
Hemorrhagic Stroke
Definitions
 Intracerebral hemorrhage
 Intracranial hemorrhage
 Parenchymal hemorrhage
 Intraparenchymal hematoma
 Contusion
 Subarachnoid hemorrhage
Cerebral Hemorrhage
Epidural hemorrhage
 Smooth onset
 Arterial origin
 Mass effect causes
coma over hours
 Similar (but slower in
evolution) to
hemorrhage in basal
ganglia
Subdural hemorrhage
 Smooth onset
 Venous origin
 May be recurrent
 Fluctuating, falsely
localizing signs
Hemorrhagic Stroke
 Rupture of vessel
 Sudden
 Active
 Fatal
 HTN
 Trauma
 Varied manifestations
Hemorrhagic Stroke
 Intracerebral
Hemorrhage
 Subarachnoid
Hemorrhage
Pathophysiology
Hemorrhagic Stroke
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Changes in vasculature
Tear or rupture
Hemorrhage
Decreased perfusion
Clotting
Edema
Increased intracranial pressure
Cortical irritation
Mom: Bowel/bladder
Reasoning/judgment
Long term memory
Voluntary
Motor
Legs
Arms
Sensations
Pain & Touch
Taste
Head
Hearing/association
& Smell & taste
Short term Memory
Vision &
visual
memory
Balance,
Coordination of each
muscle group
CN 5,6,7,8
P,R, B/P
CN 9,10,11,12
Tracks cross over
Coordinate
movement,
HR,B/P
Vessels of the Brain
Vessels of the Brain
Right Side
Circle of Willis
Physiology
Normal Cerebral Blood Flow
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Oxygen
Glucose
20% of Cardiac Output / oxygen
Arterial supply to the brain:
 Internal carotid (anteriorly)
 Vertebral arteries (posteriorly)
 Venous drainage
 2 sets of veins - venous plexuses
 Dural sinuses to internal jugular veins
 Sagittal sinus to vertebral veins
 No valves, depend on gravity and venous pressure
gradient for flow
Risk Factors
NON-MODIFIABLE
MODIFIABLE
 Age
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 2/3 over 65
 Gender
 M=F
 Female>fatality
 Race
 AA > hispanics, NA
 Asians > hem
 Heredity
 Family history
 Previous TIA/CVA
Hypertension
Diabetes mellitus
Heart disease
A-fib
Asymptomatic carotid stenosis
Hyperlipidemia
Obesity
Oral contraceptive use
Heavy alcohol use
Physical inactivity
Sickle cell disease
Smoking
Procedure precautions
Etiology
Ischemic Stroke
Embolism
Prothrombotic states
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 Hemostatic regulatory
Atrial fib
Sinoatrial Disease
Recent MI
Endocarditis
Cardiac tumors
Valvular heart disease
Patent foramen ovale
Carotid/basilar artery stenosis
Atherosclerotic lesions
Vasculitis
protein abnormalities
 Antiphospholipid
antibodies
 Hep cofactor II
Etiology
Hemorrhagic Stroke
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Chronic HTN**
Cerebral Amyloid Angiopathy*
Anticoagulation*
AVM
Ruptured aneurysm (usually subarachnoid)
Tumor
Sympathomimetics
Infection
Trauma
Transformation of ischemic stroke
Physical exertion, Pregnancy
Post-operative
Aneurysm
 Localized dilation of arterial lumen
 Degenerative vascular disease
 Bifurcations of circle of Willis
 85% anterior
 15% posterior
Aneurysm
Subarachnoid Hemorrhage
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SAH
Mortality 70%
97% HA
Nuchal rigidity
Fever
Photophobia
Lethargy
Nausea
Vomiting
Aneurysm/SAH
 Complications
 HCP
 Vasospasm
 Triple H Therapy
 HTN
 Hemodilution
 Hypervolemia
 Surgical treatment
 Clip
 Coil
 INR
Nursing Management
 Assessment
 Monitoring
 BP
 TCDs
 CBC
 Preventing complications
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Bowel program
DVT prophylaxis
Seizure prophylaxis
Psychological support
Discharge planning
Arteriovenous Malformations
 AVM
 Tangled mass of arteries and veins
 Seizure or ICH
Presentation
 Sudden onset
 Focal neurological deficit
 Progresses over minutes to hours
 HA, N/V, <<LOC, HTN
 Depends on location
Treatment of AVM
 Endovascular
 Neurosurgery
 Radiosurgery
Manifestations
by Vessel
 Vertebral Artery
 Pain in face, nose, or eye
 Numbness and weakness of face (involved side)
 Gait disturbances
 Dysphagia
 Dysarthria (motor speech)
Manifestations
by Vessel
 Internal carotid artery
 Contralateral paralysis (arm, leg, face)
 Contralateral sensory deficits
 Aphasia (dominant hemisphere involvement)
 Apraxia (motor task),
 Agnosia (obj. recognition),
 Unilateral neglect (non-dominant hemisphere
involvement)
 Homonymous hemianopia
Initial Stroke Assessment/Interventions
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Neurological assessment & NIH assessment
Call “Stroke Alert” Code
Ensure patient airway
VS
IV access
Maintain BP within parameters
Position head midline
HOB 30 (if no shock/injury)
CT, blood work, data collection/NIH Stroke Scale
Anticipate thrombolytic therapy for ischemic stroke
NIH Stroke Scale Score
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Standardized method
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measures degree of stroke r/t impairment and change in a patient over time.
Helps determine if degree of disability merits treatment with tPA.
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As of 2008 stroke patients scoring greater than 4 points can be treated with tPA.
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Standardized research tool to compare efficacy stroke treatments and rehabilitation
interventions.
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Measures several aspects of brain function, including consciousness, vision, sensation,
movement, speech, and language not measured by Glasgow coma scale.
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Current NIH Stroke Score guidelines for measuring stroke severity:
Points are given for each impairment.
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0= no stroke
1-4= minor stroke
5-15= moderate stroke
15-20= moderate/severe stroke
21-42= severe stroke
A maximal score of 42 represents the most severe and devastating stroke.
Comic Relief
Question
 The neurologic functions that are affected by
a stroke are primarily related to
 A. the amount of tissue area involved.
 B. the rapidity of the onset of symptoms.
 C. the brain area perfused by the affected artery.
 D. the presence or absence of collateral
circulation.
Question
 A patient is admitted to the hospital with a
left hemiplegia. To determine the size and
location and to ascertain whether a stroke is
ischemic or hemorrhagic, the nurse
anticipated that the health care provider will
request a
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A. CT scan.
B. lumbar puncture.
C. cerebral angiogram.
D. PET scan.
Diagnosis
Tests for the Emergent Evaluation of the Patient with Acute
Ischemic Stroke
 CT head (-)
 Electrocardiogram
 Chest x-ray
 Hematologic studies (complete blood count, platelet count,
prothrombin time, partial thromboplastin time)
 Serum electrolytes
 Blood glucose
 Renal and hepatic chemical analyses
 National Institute of Health Scale (NIHSS) score
Diagnosis
Ischemic Stroke
Hemorrhagic Stoke
Medical Management
 BP
 MAP
 CPP
 Fluid management
 euvolemia
 Seizure prophylaxis
 Factor VII, Vit K, FFP
 ICP
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HOB
Sedation
Osmotherapy
Hyperventilation
Paralytics
 Keppra
 Dilantin
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Sedation
Body temperature
PT/OT/ST
DVT prophylaxis
Treatment
Ischemic
Hemorrhagic
 Medical management
 Medical management
 TPA
 Decompression
 Craniotomy
 Endovascular
 Carotid endarectomy
 Craniectomy
 Merci clot removal
 http://youtu.be/P2TNz-TniIA
PT/OT/ST
REHABILITATION
Medications
 Anti-coagulants – A fib & TIA
 Antithrombotics
 Calcium channel blockers – Nimotop (nimodipine)
 Corticosteroids ???
 Diuretics – Mannitol, Lasix (Furosemide)
 Anticonvulsants – Dilantin (phenytoin) or Cerebyx
(Fosphenytoin Sodium Injection)
 Thrombolytics - tPA (recombinant tissue plasminogen
activator)
Medications
 Thrombolytics Recombinant Alteplase (rtPA)
Activase, Tissue plasminogen activator
 Treatment must be initiated promptly after CT to R/O
bleed
 Systemic within 3 hours of onset of symptoms
 Intra-arterial within 6 hours of symptoms
 Some exclusions:
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Seizure at onset
Subarachnoid hemorrhage
Trauma within 3 months
History of prior intracranial hemorrhage
AV malformation or aneurysm
Surgery 14 days, pregnancy,
Cardiac cath. 7 days
Neurosurgical Management
 Craniotomy
 Craniectomy
 EVD placement
 ICP monitor placement
Recommendations for Surgical
Treatment of ICH
 Nonsurgical candidates
 Surgical candidates
 Small hemorrhage
 >3cm
 Minimal deficit
 Neuro deficit
 Brain stem compression
 MLS, HCP
 Aneurysm, AVM,
cavernous hemangioma
 GCS </= 4 (unless brain
stem compression)
 Loss of brainstem reflexes
 Severe coagulopathy
 Basal ganglion or thalamic
 Young c mod/large lobar
hemorrhage c clinical
deterioration
Reducing Primary Risk
 Obstructive sleep apnea
 Homocysteine  folate, B6, B12
 Hypertension – morning BP surge
 Smoking  50% risk reduction in 1 yr
 Hyperlipidemia  statins
 Migraine  triptans
 Drugs – cocaine, ephedra, PPA
Reducing Primary Risk
 Asymptomatic carotid stenosis
 Endarterectomy for > 60% stenosis
 Risk reduction for 3% to 1% per year
 Benefit related to surgical risk
 Nonvalvular atrial fibrillation
 Aspirin for patients < 65 years, healthy
 Warfarin for patients > 65 years or having other
stroke risk factors
Reducing Secondary Risk
Reducing risk of recurrence
 TIA with ipsilateral carotid stenosis 
endarterectomy for > 70% stenosis
 Cardiogenic embolism  warfarin
 Lacunar infarcts  aspirin, dipyridamole
 Cryptogenic infarcts (40% embolic) 
anticoagulation?
Reducing Risk in Children
 Sickle cell disease
 Screen with transcranial doppler q 6 mo
 Transfusion therapy for 2 abnormal studies
 Congenital heart disease
 Arterial dissections (trauma)
 Prothrombotic disorders
 Mitochondria disorders (MELAS)
Using Statins
 Pooled results after 5 years
 Pravastatin or Simvastatin 40 mg/day
 Changes in cholesterol levels
 Total cholesterol decreased 20%
 LDL cholesterol decreased 28%
 HDL cholesterol increased 5%
 Triglycerides decreased 13%
Using Statins
 Reducing LDL cholesterol by 1 mmol/L
 22% stroke reduction in patients with known
vascular disease
 6% stroke reduction in patients without known
vascular disease
 28% reduction in thromboembolic stroke
Complications
 Increased intracranial pressure
 Rebleeding
 Vasospasm
 HCP
 Death
Outcomes
 Age
 Size, volume
 Location
 HCP, IVH
 Deficit, LOC, MAP
 Duration
 Co-morbidities
 44% mortality
References
 AANN Core Curriculum for Neuroscience Louis, MO.
Nursing, 4th Ed. 2004. Saunders. St.
 Broderick, J., et. al. (1999) Guidelines for the
management of spontaneous intracerebral
hemorrhage. AHA.
 El-Mitwali, A., Malkoff, M. (2001) Intracerebral
hemorrhage. The Internet Journal of
Neurosurgery. 1.1.
 Greenberg, Mark. (2006). Handbook of
Neurosurgery. Greenberg Graphics,
Tampa, Florida.